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RAP1B, a DVL2 binding protein, activates Wnt/beta-catenin signaling in esophageal squamous cell carcinoma

Zhao Jia1, Yang Yang1, Zhu Dengyan1

  • 1Department of Thoracic Surgery, The First Affiliated Hospital, Zhengzhou University, Henan province, PR China; Department of Key Thoracic Tumour Experimental Laboratory of Zhengzhou, PR China.

Gene
|January 26, 2017
PubMed

Insights

RAP1B protein promotes esophageal squamous cell carcinoma (ESCC) growth and metastasis. Targeting RAP1B may offer a new therapeutic strategy for ESCC treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • RAP1B, a small GTPase, is implicated in various cellular functions and upregulated in cancers.
  • Previous research suggests miR-518 targets RAP1B in esophageal squamous cell carcinoma (ESCC), but RAP1B's role in ESCC requires further elucidation.

Purpose of the Study:

  • To investigate the expression pattern and functional significance of RAP1B in esophageal squamous cell carcinoma (ESCC).
  • To explore the underlying molecular mechanisms by which RAP1B influences ESCC progression.

Main Methods:

  • Analysis of RAP1B expression in ESCC clinical samples.
  • In vitro gain-of-function and loss-of-function assays to assess RAP1B's impact on ESCC cell behavior.
  • Mechanistic studies involving protein-protein interactions and signaling pathway analysis.

Main Results:

  • RAP1B expression is significantly upregulated in ESCC tissues.
  • Elevated RAP1B expression enhances ESCC cell proliferation, migration, and metastasis.
  • RAP1B interacts with DVL2, activating the beta-catenin/TCF signaling pathway.

Conclusions:

  • RAP1B plays a crucial oncogenic role in the development and progression of ESCC.
  • RAP1B's activation of the beta-catenin/TCF pathway contributes to its pro-tumorigenic effects.
  • RAP1B represents a potential therapeutic target for esophageal squamous cell carcinoma.
Keywords:
Beta-catenin/TCF signalingCell growth and migrationESCCRAP1B

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